{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T18:17:08Z","timestamp":1782325028492,"version":"3.54.5"},"reference-count":37,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>The direct action of aldosterone (10<jats:sup>\u221212<\/jats:sup>M) on net bicarbonate reabsorption ( J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>) was evaluated by stationary microperfusion of an in vivo middle proximal tubule (S2) of rat kidney, using H ion-sensitive microelectrodes. Aldosterone in luminally perfused tubules caused a significant increase in J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>from a mean control value of 2.84 \u00b1 0.08 [49\/19 ( n\u00b0 of measurements\/ n\u00b0 of tubules)] to 4.20 \u00b1 0.15 nmol\u00b7cm<jats:sup>\u22122<\/jats:sup>\u00b7s<jats:sup>\u22121<\/jats:sup>(58\/10). Aldosterone perfused into peritubular capillaries also increased J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>, compared with basal levels during intact capillary perfusion with blood. In addition, in isolated perfused tubules aldosterone causes a transient increase of cytosolic free calcium ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>), monitored fluorometrically. In the presence of ethanol (in similar concentration used to prepare the hormonal solution), spironolactone (10<jats:sup>\u22126<\/jats:sup>M, a mineralocorticoid receptor antagonist), actinomycin D (10<jats:sup>\u22126<\/jats:sup>M, an inhibitor of gene transcription), or cycloheximide (40 mM, an inhibitor of protein synthesis), the J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>and the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>were not different from the control value; these drugs also did not prevent the stimulatory effect of aldosterone on J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. However, in the presence of RU 486 alone [10<jats:sup>\u22126<\/jats:sup>M, a classic glucocorticoid receptor (GR) antagonist], a significant decrease on J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>was observed; this antagonist also inhibited the stimulatory effect of aldosterone on J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. These studies indicate that luminal or peritubular aldosterone (10<jats:sup>\u221212<\/jats:sup>M) has a direct nongenomic stimulatory effect on J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>and on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in proximal tubule and that probably GR participates in this process. The data also indicate that endogenous aldosterone stimulates J<jats:sub>HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup><\/jats:sub>in middle proximal tubule.<\/jats:p>","DOI":"10.1152\/ajprenal.90217.2008","type":"journal-article","created":{"date-parts":[[2009,2,19]],"date-time":"2009-02-19T02:09:41Z","timestamp":1235009381000},"page":"F1185-F1193","source":"Crossref","is-referenced-by-count":17,"title":["Direct action of aldosterone on bicarbonate reabsorption in in vivo cortical proximal tubule"],"prefix":"10.1152","volume":"296","author":[{"given":"Patricia Silva","family":"Pergher","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deise","family":"Leite-Dellova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margarida","family":"de Mello-Aires","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"R1","unstructured":"Alpern RJ.Renal acidification mechanisms. 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